Outline

Objective

Cannabinoid ligands are supposed to exert neuroprotective mechanisms after traumatic brain injury (TBI). The mechanisms underlying this neuroprotection are not yet clear, and they may include vascular and non-vascular actions. The pursuit of the study was, therefore, to characterise cannabinoid mediated cerebrovascular relaxation following experimental focal or global cerebral trauma in male Sprague-Dawley rats.

Results

In MCA segments relaxation upon Meth-A was significantly enhanced, mainly with respect to the affinity after TBI. This increase was apparent in the segments taken from the proximal and the distal part. The pD2 values (meanÂ±SD) obtained in the distal segments after CL were 5.47Â±0.36 (CL, 24h) and 5.36Â±0.24 (CL, 48h), 5.49Â±0.16 (WD, 24h) and 5.48Â±0.31 (WD, 48h). All values are significantly higher than the control value (4.99Â±0.17). In the BA there was no significant shift of the pD2 value after TBI, while in the MA the affinity of Meth-A was unaltered (after CL) or decreased (after WD). The maximum relaxation obtained in MCA segments was slightly increased after CL and significantly augmented after WD, unaltered after both, CL and WD trauma in the BA, and significantly attenuated in the MA after focal and global TBI.

Conclusions

After focal and global TBI cerebrovascular reactivity upon Meth-A was maintained or even enhanced, while it was diminished in the MA. These alterations suggest that the cannabinoid system may be a new therapeutic approach for the treatment of TBI patients. In addition, the results strongly suggest systemic alterations in vascular function to occur after head injury. The pathophysiological role of these systemic alterations needs to be further addressed.